Cibert C, Prulière G, Lacombe C, Deprette C, Cassoly R
Laboratoire de Biologie du Développement, Institut Jacques Monod, UMR 7592, CNRS, Universités Paris VI et Paris VII, F-75005 Paris, France.
Biophys J. 1999 Mar;76(3):1153-65. doi: 10.1016/S0006-3495(99)77280-2.
Human red blood cells contain all of the elements involved in the formation of nonmuscle actomyosin II complexes (V. M. Fowler. 1986. J. Cell. Biochem. 31:1-9; 1996. Curr. Opin. Cell Biol. 8:86-96). No clear function has yet been attributed to these complexes. Using a mathematical model for the structure of the red blood cell spectrin skeleton (M. J. Saxton. 1992. J. Theor. Biol. 155:517-536), we have explored a possible role for myosin II bipolar minifilaments in the restoration of the membrane skeleton, which may be locally damaged by major mechanical or chemical stress. We propose that the establishment of stable links between distant antiparallel actin protofilaments after a local myosin II activation may initiate the repair of the disrupted area. We show that it is possible to define conditions in which the calculated number of myosin II minifilaments bound to actin protofilaments is consistent with the estimated number of myosin II minifilaments present in the red blood cells. A clear restoration effect can be observed when more than 50% of the spectrin polymers of a defined area are disrupted. It corresponds to a significant increase in the spectrin density in the protein free region of the membrane. This may be involved in a more complex repair process of the red blood cell membrane, which includes the vesiculation of the bilayer and the compaction of the disassembled spectrin network.
人类红细胞包含非肌肉肌动球蛋白II复合物形成过程中涉及的所有元素（V. M. 福勒。1986年。《细胞生物化学杂志》31:1 - 9；1996年。《当代细胞生物学观点》8:86 - 96）。这些复合物尚未明确的功能。利用红细胞血影蛋白骨架结构的数学模型（M. J. 萨克斯顿。1992年。《理论生物学杂志》155:517 - 536），我们探讨了肌球蛋白II双极微丝在恢复膜骨架方面可能的作用，膜骨架可能因重大机械或化学应激而局部受损。我们提出，局部肌球蛋白II激活后，远处反平行肌动蛋白原纤维之间建立稳定连接可能启动受损区域的修复。我们表明，可以确定这样的条件，即计算出的与肌动蛋白原纤维结合的肌球蛋白II微丝数量与红细胞中存在的肌球蛋白II微丝估计数量一致。当定义区域中超过50%的血影蛋白聚合物被破坏时，可以观察到明显的修复效果。这对应于膜的无蛋白区域血影蛋白密度的显著增加。这可能参与了红细胞膜更复杂的修复过程，该过程包括双层膜的小泡化和拆解的血影蛋白网络的压实。
